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Medical Studies 1 > Resp Week 8 > Flashcards

Resp Week 8 Flashcards

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USMLE® Step 1 flashcards
1
Q

describe the epidemiology of SARS-CoV-2 in regards to virus factors

A

virus genome mutates, leading to changes in viral proteins

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2
Q

describe the epidemiology of SARS-CoV-2 in regards to virus transmission

A

zoonotic infection

respiratory transmission

faecal-oral transmission

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3
Q

describe the epidemiology of SARS-CoV-2 in regards to host factors

A

receptors expressed by different hosts, ACE2, contact w animals, air travel and other human behaviours

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4
Q

outline the pathophysiology of SARS-CoV-2

A

infection of endothelial cells

then, spread of virus

then, innate immune response

then, cytokine storm

then, ARDS

then, activation of ACE-2

then, post COVID symptoms

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5
Q

what are the two phases of COVID19 infection

A

rapid viral propagation

uncontrolled inflammatory responses (cytokine storm)

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6
Q

what are 4 stages of the rapid viral propagation phase of COVID19 infection

A

exposure and entry

initial replication

symptom onset

viral shedding

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7
Q

what happens during exposure and entry in rapid viral propagation of COVID19

A

infection begins w exposure to SARS-CoV-2 virus, which then enters body through respiratory tract

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8
Q

what happens during initial replication in rapid viral propagation of COVID19

A

virus rapidly replicates in the upper respiratory tract, and then spreads to the lower respiratory tract where it can infect the lungs

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9
Q

what happens during symptom onset in rapid viral propagation of COVID19

A

many may remain asymptomatic or experience mild to moderate symptoms e.g fever, cough, sore throat, loss of taste/smell

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10
Q

what happens during viral shedding in rapid viral propagation of COVID19

A

infected individuals can shed virus and are contagious during this phase, contributing to spread of disease to others

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11
Q

describe what happens during the uncontrolled inflammatory responses (cytokine storm)

A

virulence often accompanied by programmed cell death

this contributes to clearance of infected cells from body thus preventing further replication of virus

however PCD releases pro-inflammatory cytokines in high quantities leading to what is known as a cytokine storm (e.g PAMPs, DAMPs and cellular cytokines)

the disregulated release of pro inflammatory mediators leads to end organ damage

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12
Q

what are 7 common symptoms associated w COVID 19

A

fever

cough

fatigue

anosmia

sore throat

dyspnea

headache

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13
Q

outline acute respiratory distress syndrome (ARDS)

A

during the second phase of COVID19, body can enter acute respiratory distress whereby its pneumocytes lose the ability to secrete surfactant

this is due to physiological and structural changes in the lung tissue itself, due to acute lung injury at the hands of dysregulated pro inflammatory cytokine release

can lead to tachypnoea, dyspnoea, low blood o2, rattling sounds upon auscultation of lungs

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14
Q

what are 4 prevention methods for COVID 19

A

social distancing

mask wearing

vaccination

hand hygiene

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15
Q

what are 3 pharmacological treatments for management of COVID19

A

analgesics

antivirals

O2 therapy

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16
Q

what are 5 aetiological classifications of pneumonia

A

bacterial - often streptococcus pneumoniae

viral - such as influenza or RSV

aspiration - foreign material, typically gastric contents

atypical - pathogens such as mycoplasma or chlamydia

opportunistic - individuals w weakened immune systems

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17
Q

what are 3 acquisition based classifications of pneumonia

A

community acquired - outside of healthcare settings often caused by common bacteria/viruses

healthcare acquired - during or after hospitalisation/healthcare settings often involving drug-resistant bacteria

ventilator associated - Pt on mechanical ventilation often due to hospital acquired infections

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18
Q

what are 8 symptoms/signs of pneumonia

A

productive cough

dyspnea

pleuritic chest pain

hypoxia

dullness to percussion

decreased breath sounds

bronchial breathing

coarse crackles

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19
Q

outline the pathophysiology of pneumonia

A

underlying agent e.g bacteria, virus etc

then, colonisation of nasopharynx

then, micro-aspiration

then, colonisation of lung parenchyma

then, programmed cell death

then, release of pro-inflammatory cytokines

then, systemic inflammatory response

then, end organ and systemic inflammatory-associated damage

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20
Q

what are 5 complications of pneumonia

A

sepsis

lung abscess

respiratory failure

kidney failure

neurological effects

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21
Q

describe the severity parameters for pneumonia

A

SMART-COP criteria:
systolic BP < 90
multi lobar CXR involvement
albumin <3.5
resp rate >30/min
tachycardia
confusion
O2 sat <90
pH <7.35

5-6 points = high risk of needing IRVS
7+ points = v high risk of needing IRVS

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22
Q

outline the investigative process in diagnosing pneumonia

A

complete blood count - looking for high white cell count and raised inflammatory markers

EUCA - looking for renal fn implications

viral swab - looking for presence of underlying viral contributor

sputum MCS - looking for bacterial contributors

CXR - looking for consolidation and empyema

bronchoscopy

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23
Q

describe the role of bronchoscopy in the investigation of pulmonary infection

A

use of flexible camera and attached suction device to suck out mucous from the lungs

enters via oral or nasal cavity

24
Q

what are 4 management options for pneumonia

A

antibiotics

symptomatic alleviation

supportive management

nutrition assessment

25
Q

outline the pathogenesis of tuberculosis

A

M.tuberculosis enters the upper airways

then, attempted phagocytosis by alveolar macrophages

then, M.tuberculosis migrates to lymph nodes and activates B and T cells OR if it survives then it migrates to lung parenchyma

then, B and T cells enable macrophages to differentiate into epithelioid cells

then, there is fusion of epithelioid cells to form granuloma

then, granuloma encases M.tuberculosis preventing its spread and proliferation

26
Q

what are two characteristics of M.tuberculosis that make it trickier to treat

A

slow growth

waxy cell wall

27
Q

what are 8 symptoms/signs of TB

A

chronic cough

haemoptysis

chest pain

dyspnea

loss of appetite

night sweats

fatigue

pallor, wasted appearance and clubbing upon general inspection

28
Q

what are 5 extrapulmonary signs/symptoms of TB

A

haematuria - due to TB of kidney

headache - due to TB meningitis

back pain - due to TB of spine

hoarseness - due to TB of larynx

abdominal discomfort - peritoneal TB

29
Q

what are 4 investigations that can be done in the diagnosis of TB

A

sputum microscopy

sputum culture

drug sensitivity

CXR

30
Q

what are 6 common complications of TB

A

pleural effusion

haematogenous TB

cardiac TB

ocular TB

hepatic TB

GI TB

31
Q

what is the recommended management for bacterial pneumonia

A

Rx w specific antibiotics (e.g amoxycillin for S.pneumoniae)

32
Q

what is the recommended management for viral pneumonia

A

Rx w oseltamivir (antiviral) ONLY in cases of individuals w risk factors for poor outcomes of influenza (e.g pregnant) and then cease immediately when influenza is ruled out

33
Q

what is the recommended management for TB in the intensive phase (bactericidal)

A

Rx for 2 months:

isoniazid

rifampicin

pyrazinamide

ethambutol

34
Q

what is the recommended management for TB in the continuation phase (sterilisation)

A

Rx for 4 months:

isoniazid

rifampicin

35
Q

what is directly observed therapy (DOT)

A

describes administration of therapy in a way that is observable by the practitioner

enables compliance

recommended for individuals w cultural barriers, mental or cognitive pathologies, or those who are at high risk of fatal consequences

36
Q

describe acute vs chronic chest infection

A

acute = <3 weeks / anything longer = chronic

chronic is characterised by stability and interruptions by exacerbations

pathogenesis of chronic chest infection is a vicious cycle (it results from the inflammation and creates a cycle towards further infection in the chronically damaged lung)

37
Q

what are 4 risk factors for chronic chest infection

A

inability to clear secretions

reduced respiratory effort

decreased cough or gag reflex

immunocompromised patients

38
Q

what are 4 symptoms of persistent chest infection

A

productive cough

malaise

chest pain

fever

39
Q

what are 6 Rx methods for management of persistent chest infection

A

antibiotics

airway clearance

vaccination

education

smoking cessation

emergency pack use

40
Q

describe the pathogenesis of bronchiecstasis

A

impaired drainage/obstruction - impairment of mucus clearance and drainage within airways due to structural abnormalities leading to mucus accumulation and bacterial growth

host response - body’s immune system mounts prolonged defence, contributing to tissue damage and the perpetuation of the condition

transmural inflammation - inflammation that extends through the full thickness of the airway wall, leading to structural changes in the bronchi and bronchioles

41
Q

outline the pathophysiology of bronchiectasis

A

acquired immunodeficiency, autoimmune, congenital, endobronchial obstruction, or other factors such as inhalation exposure or COPD leads to irreversibly dilated bronchi, chronic bronchial infection and inflammation and easily collapsible airways, resulting in bronchiectasis

42
Q

what are 5 signs/symptoms of bronchiectasis

A

productive cough

dyspnea

sleep disturbances

changes in appetite

systemic infection

43
Q

what are 5 investigative processes that can be done in the diagnosis of bronchiectasis

A

history/exam

sputum culture

CXR

lung function test

CBE

44
Q

what are 5 general management methods for bronchiectasis

A

physical therapy

positive airway pressure

antibiotic therapy

pulmonary rehab

smoking cessation

45
Q

describe the epidemiology of cystic fibrosis

A

3538 ppl living with CF

median age of diagnosis is 20.2 years

CF is most common life-limiting disease in australia

CF is predominantly inherited by caucasians

46
Q

describe class 1 CF

A

caused by a mutation that results in the absence of functional CFTR protein, leading to severe disease w minimal to no CFTR activity

47
Q

describe class 2 CF

A

associated w mutations that result in defective CFTR protein processing and reduced function, causing moderate to severe symptoms

48
Q

describe class 3 CF

A

involves mutations leading to partially functional CFTR protein, resulting in variable and typically milder disease symptoms

49
Q

describe class 4 CF

A

characterised by mutations causing normal CFTR protein production, but w impaired function, resulting in mild or atypical CF symptoms

50
Q

describe class 5 CF

A

involves mutations that affect CFTR regulation and function, leading to mild or atypical CF symptoms

51
Q

describe class 6 CF

A

associated w mutations causing reduced CFTR protein stability, resulting in mild or atypical symptoms w residual CFTR function

52
Q

what is the effect of dysfunctional CFTR on the respiratory system

A

result in production of thick and sticky mucus in airways, making it difficult to clear mucus

this leads to chronic airway obstruction, recurrent lung infections, and progressive lung damage

53
Q

what is the effect of dysfunctional CFTR on the digestive system

A

affects the pancreas, reducing its ability to release enzymes necessary for digestion

this leads to malabsorption of nutrients, malnutrition, and GI issues

54
Q

what is the effect of dysfunctional CFTR on the glandular system

A

leads to salty-tasting skin due to elevated salt levels in sweat, which is a diagnostic feature of CF

55
Q

what is the effect of dysfunctional CFTR on the reproductive system

A

can cause infertility in both males and females due to issues w production and transport of reproductive fluids

56
Q

describe how genotype can inform management of CF

A

genotype testing IDs specific mutations in the CFTR gene, allowing healthcare providers to determine the exact genetic profile of an individual w CF

it can also guide the selection of mutation-specific medications and therapies

allows for tailored and optimal treatment

57
Q

what are 3 management methods for treatment of CF

A

symptomatic therapy

CFTR modulator drugs

genetic therapies

Medical Studies 1 (16 decks)

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